[Fungal infection of the small bowel mucosa].
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Biomedical subjects
Publications and source records attributed to B Müller.
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[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
In pregnant women with E-gestosis distribution and elimination of furosemid are significantly different to a non-pregnant control group. Furosemid guarantees a rapid and safe excretion of edemas. The efficiency of furosemid concerning electrolyte excretion is stronger in pregnant women with E-gestosis than in nonpregnant women. Therefore furosemide should be administered to pregnant women under intensive electrolyte control only.
In intestinal specimens of children repeatedly attacked by enteritis electron microscopic investigations were practiced. In 26% of biopsies mycosis was found and in 72% a bacterial infection of the intestinal mucosa. We found narrow contacts between the infectious agents and the mucosa by electron microscopic evaluation (adhesion, penetration, partly thick layers). The microbes found are suitable to maintain the recurring cases of diarrhoea. Our results demand an exact antibiotic and antimycotic therapy.
Cardio-hemodynamic and direct cardiac effects of 1-(m-methoxyphenyl)-2-(dimethylaminomethyl)- cyclohexan -1-ol (tramadol, Tramal ), and pentazocine were investigated in anaesthetized rabbits and in isolated guinea-pig atria and papillary muscles. Tramadol in anaesthetized rabbits at 1 and 4.64 mg/kg i.v. slightly increased arterial blood pressure and heart rate and at 10 mg/kg i.v. transiently decreased blood pressure, LV dp/dtmax and cardiac output and increased LV enddiastolic pressure. Pentazocine at 1 mg/kg i.v. increased blood pressure and peripheral vascular resistance, while with 2.15 and 4.64 mg/kg exerted dose-dependent cardiodepressive effects with initial fall of blood pressure, heart rate, LV dp/dtmax and cardiac output and increase of LV enddiastolic pressure. In spontaneously beating atria and electrically driven papillary muscles tramadol in the concentration range from 1 X 10(-6)-1 X 10(-4) mol/l showed concentration-dependent positive inotropic effects which where abolished and reversed to negative inotropic actions in catecholamine-depleted papillary muscles. In contrast, pentazocine in the same concentration range showed pure negative inotropic and negative chronotropic effects which were intensified in catecholamine-depleted papillary muscles. These in vitro results suggest that both tramadol and pentazocine interact with endogenous catecholamines in a way counteracting direct negative inotropic effects. While in the case of tramadol the sum of both properties leads to positive inotropic effects at least in vitro, with pentazocine negative inotropic action prevails.
If erythrocytes were transferred into solutions of different ionic composition, they changed the inner pH and chloride concentration until reaching a new quasi-equilibrium state (C-State). Electrochemical measurements were performed to follow the kinetics of this adaption and to answer the question whether the time constant of unidirectional chloride flux or time constant of chloride net flux is responsible for this process. It was found that the kinetics depend strongly on the kind and the concentration of the buffer system used. In unbuffered solutions, a new Cl-pH-equilibrium is reached very fast and proceeds by the Cl-/HCO-3-exchange. If Tris or phosphate buffer were used, this process had a time constant of about 10(-3) S-1 and was mainly realised by a Cl-/OH-exchange or Cl-H+-cotransport. If the suspension contained phosphate, an overshoot of pH took place. The reason for this behavior is the additional exchange of Cl- for HPO2-(4) + H+.
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Phosphohexose-isomerase concentration in cysts and effusions of various localisations was measured in 83 cases. The enzyme activity was compared with aspiration-cytologic results on the basis of histologic diagnoses. There is a reasonable correlation from cytologic cellularity and PHI-concentration. PHI-measurements give an additional information whether an aspirated fluid derives from a benign or a malignant lesion.
Two heat-sensitive (arrested in G1 at 39.5 degrees C) and two cold-sensitive (arrested in G1 at 33 degrees C) clonal cell-cycle mutants that had been isolated from the same clone (K 21), of the murine mastocytoma P-815 cell line, were tested for thymidine kinase (EC 2.7.1.21) activity. After shift of mutant cells to the nonpermissive temperature, thymidine kinase activity decreased, and minimal levels (i.e., less than 3% of those observed for 'wild-type' K 21 cells at the respective temperature) were attained within 16 h in heat-sensitive and after 3-4 days in cold-sensitive mutants, which is in good agreement with kinetics of accumulation of heat-sensitive and cold-sensitive cells in G1 phase. After return of arrested mutant cells to the permissive temperature, thymidine kinase of heat-sensitive cells increased rapidly and in parallel with entry of cells into the S phase. In cultures of cold-sensitive cells, however, initiation of DNA synthesis preceded the increase of thymidine kinase activity by approx. one cell-cycle time. Thymidine kinase activities in revertants of the heat-sensitive and cold-sensitive mutants were similar to those of 'wild-type' cells. In 'wild-type' K 21 cells incubated at 39.5 degrees C, thymidine kinase activity was approx. 30% of that at 33 degrees C. This difference is attributable, at least in part, to a higher rate of inactivation of the enzyme at 39.5 degrees C, as determined in cultures incubated with cycloheximide. The rapid increase of thymidine kinase activity that occurred after shift of K 21 cells and of arrested heat-sensitive mutant cells from 39.5 degrees C to 33 degrees C was inhibited by actinomycin D and cycloheximide.
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We have analysed nuclear RNA from T. thermophila by RNA transfer hybridization using cloned rDNA fragments. A very high number of in vivo intermediates and by-products of rRNA processing were identified. These include putative intermediates of the splicing process and alternative products resulting from temporal variability in various endonucleolytic cleavages. In addition, four small RNA species including only transcribed spacer sequences were detected. These are (1) the IVS RNA (approximately 400 bases), the by-product of the splicing process, (2) a fragment from the internal transcribed spacer (approximately 360 bases), possibly resulting from 3'-end processing of pre-17S rRNA, (3) a fragment comprising most or all of the external transcribed spacer (approximately 600 bases) obviously representing the major by-product of 5'-end processing, and, in addition, (4) a small fragment from the initiation region (approximately 230 bases) which might be a product of premature transcription termination.
Because accurate neuronal dimensions are essential for mathematical modeling of neuronal properties, the effects of a number of salines and fixative procedures on neuronal size were compared, including the non-chemical, freeze substitution method. Using an identified neuron we compared diameters and found some of the fixative-saline combinations caused shrinkage by as much as a factor of four from our best estimates of the in vivo size from the quick frozen preparations. A glutaraldehyde based fixation procedure was found which gives results in good agreement with the frozen tissue.
Eighteen adult patients with typical history and signs of normocalcemic tetany (hyperventilation syndrome) and 18 age- and sex-matched controls were submitted to a provocation test for tetany. This consisted of 10-min ischemia of the right arm produced by suprasystolic cuff compression at the upper arm (Trousseau test) and a postischemic electromyographic recording from the right interosseous I muscle. Postischemic repetitive discharges were found in all patients and predominantly consisted of multiples of 5 times and more. These discharges lasted 8 min on the average. Of the normal controls, as many as 16 subjects (88.8%) also exhibited tetanic discharges. However, these preferred a lower number of repetitions, such as doublets or triplets. Both number of repetition and duration of postischemic tetanic activity were significant parameters discriminating between patients and controls (2P less than 0.001), as was the cumulative total number of spontaneous potentials, amounting, on the average, to 10,266 in the group of patients and to only 320 in the controls (2P less than 0.001). The investigation has shown that the occurrence of postischemic tetanic spontaneous activity per se does not help to discriminate between cases of latent tetany and healthy controls. However, a normocalcemic tetanic condition may be assumed if multiples occur with a complexity of quadruplets or more, if these multiples last at least 2 min, and if they appear in a rhythmic order and in groups.
The influence of CG 4203, a chemically and metabolically stable prostacyclin analogue, on plasma renin activity, arterial blood pressure, renal function and water intake was investigated in conscious rats. CG 4203 infused intravenously starting at 1 microgram X kg-1 X min-1 induced both a fall in blood pressure and an increase of plasma renin activity. The angiotensin II antagonist saralasine infused simultaneously intensified the hypotensive effect of CG 4203 (1.0 microgram X kg-1 X min-1). Within a similar dose range CG 4203 dose-dependently inhibited diuresis and saluresis and reduced the urinary sodium/potassium ratio. These effects were partially reversed by adrenalectomy and completely abolished by pretreatment with the angiotensin I converting enzyme inhibitor captopril. Similarly, CG 4203 (0.21 - 4.64 micrograms X kg-1 X min-1) dose-dependently caused increased water intake which was prevented by previous nephrectomy. In conclusion, it is demonstrated that CG 4203 like prostacyclin itself already at hypotensive threshold dosages stimulates a functionally relevant renin release. The activation of the renin-angiotensin-aldosterone system attenuates the intrinsic hypotensive effects of CG 4203. the antidiuretic and dipsogenic efficacy of CG 4203 can also be attributed to renin-dependent angiotensin II formation.
From a cosmid gene bank of Bacillus cereus GP4 in Escherichia coli we isolated clones which, after several days of incubation, formed hemolysis zones on erythrocyte agar plates. These clones contained recombinant cosmids with B. cereus DNA insertions of varying lengths which shared some common restriction fragments. The smallest insertion was recloned as a PstI fragment into pJKK3-1, a shuttle vector which replicates in Bacillus subtilis and E. coli. When this recombinant plasmid (pJKK3-1 hly-1) was transformed into E. coli, it caused hemolysis on erythrocyte agar plates, but in liquid assays no external or internal hemolytic activity could be detected with the E. coli transformants. B. subtilis carrying the same plasmid exhibited hemolytic activity at levels comparable to those of the B. cereus donor strain. The hemolysin produced in B. subtilis seemed to be indistinguishable from cereolysin in its sensitivity to cholesterol, activation by dithiothreitol, and inactivation by antibodies raised against cereolysin. When the recombinant DNA carrying the cereolysin gene was used as a probe in hybridization experiments with chromosomal DNA from a streptolysin O-producing strain of Streptococcus pyogenes or from listeriolysin-producing strains of Listeria monocytogenes, no positive hybridization signals were obtained. These data suggest that the genes for these three SH-activated cytolysins do not have extended sequence homology.
A series of prostacyclin analogues were synthesized and investigated for influence on blood pressure in rats, in vivo inhibition of platelet aggregation in rats, and in vitro inhibition of platelet aggregation in human platelet-rich plasma. The common feature of the analogues described is a replacement of C1-C4 of prostacyclin by a carboxyphenylene residue. The following structure-activity relationships were obtained. Only the meta-carboxyphenylene derivatives yield substantial prostacyclin activity. The 2,3,4-trinor-1,5-inter-m-phenylene prostacyclin analogues in contrast to the natural prototype are reasonably stable against hydrolysis of the enolether bond. The corresponding 2,3,4-trinor-1,5-inter-m-phenylene analogues of carbaprostacyclin have a somewhat lower specific activity but are superior in stability at acid pH values. With regard to the stereoisomerism at the delta 5 double bond, the Z-isomers of the oxa-cyclic prostacyclin series and the E-isomers of the carba-cyclic prostacyclin series are substantially more active than their counterparts. As with natural prostacyclin, the OH group at C15 has to be present in S-configuration. The "wrong" isomers do not inhibit prostacyclin-dependent effects. Resistance against 15-hydroxyprostaglandin dehydrogenase is achieved by substitutions at or near C15. Optimum specific activity combined with resistance against all known prostaglandin-activating enzymes is observed in prostacyclin and carbaprostacyclin analogues, in which the terminal n-pentyl residue is replaced by cyclohexyl. Duration of action, i.e. lowering of blood pressure in anaesthesized rats and inhibition of platelet aggregation in anaesthesized rats, was investigated with selected analogues in order to check the consequences of chemical and metabolic stabilization.(ABSTRACT TRUNCATED AT 250 WORDS)
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